Asthma is a chronic inflammatory pulmonary disease and respiratory syncytial virus (RSV) infection is a common cause of lower respiratory tract illness in infants and young children. α-Asarone presents many pharmacological effects and has been demonstrated to be useful in treating asthma. However, the functional mechanism of α-asarone in RSV-infected asthma has not been investigated. Long non-coding RNAs (lncRNAs) have been reported to play critical roles in many biological processes. Although many lncRNAs have been characterized, few were reported in asthma, especially in RSV-induced asthma. Currently, a novel post-transcriptional regulation has been proposed in which lncRNAs function as competing endogenous RNAs (ceRNAs) to competitively sponge miRNAs, thereby regulating the target genes. In the present study, we established an RSV-infected Sprague-Dawley rat model and demonstrated that lncRNA-PVT1 is involved in the mechanism of α-asarone in treating RSV-induced asthma, and lncRNA-PVT1 regulates the expression of E2F3 by functioning as a ceRNA which competitively sponges miR-203a.

Asthma is one of the most common chronic inflammatory diseases. Although the scorpion and centipede (SC) significantly ameliorates asthma and changes exosomal miRNAs, the molecular mechanism is still obscure. Here, we show that SC improves inflammation in asthmatic mice and increases M2 macrophage-derived exosomes (M2Φ-Exos) by promoting M2 macrophage polarization. The M2Φ-Exos remarkably inhibits airway epithelial cell pyroptosis by reducing the expression of NLRP3, caspase-1, and LI-1β and mitochondrial swelling. Furthermore, miR-30b-5p is up-regulated in M2Φ-Exos compared with M1Φ-Exos. Overexpression of miR-30b-5p in M2Φ-Exos prevents airway epithelial cell pyroptosis, while down-regulation of miR-30b-5p promotes pyroptosis. We also uncover that pyroptosis is increased in asthmatic mice, while SC blocks pyroptosis. Moreover, miR-30b-5p overexpressed M2Φ-Exos further enhances the ameliorative effect of SC, which significantly down-regulates IRF7 expression. Our results collectively reveal that M2Φ-Exos induced by SC could carry miR-30b-5p to mitigate severe asthma by inhibiting airway epithelial cell pyroptosis. Most importantly, our findings may provide a potential clinical application of M2Φ-Exos for treating severe asthma.

Asthma is a common respiratory disease with inflammation in the lungs. Exosomes and microRNAs (miRNAs) play crucial role in inflammation, whereas the role of exosomal miRNA in asthma remains unknown. Here, we aimed to identify the key exosomal miRNAs and their underlying mechanisms involved in scorpio and centipede (SC) treatment in asthma. Eighteen mice were randomly divided into three groups: control group, asthma group, and SC treatment group. Effect of SC was assessed by hematoxylin-eosin staining and real-time PCR. Exosomes from asthma and SC treatment groups were analyzed by small RNA-seq. Results revealed SC significantly alleviated the pathogenesis of asthma and suppressed the release of inflammatory cytokines. A total of 328 exosomal miRNAs were differentially expressed between the exosomes from asthma and SC-treated mice, including 118 up- and 210 downregulated in SC-treated mice. The altered exosomal miRNAs were primarily involved in the function of transcription, apoptotic process, and cell adhesion; and pathway of calcium, Wnt, and MAPK signaling. Real-time PCR verified exosomal miR-147 was downregulated, while miR-98-5p and miR-10a-5p were upregulated in SC-treated mice compared to asthma mice. Moreover, the target genes of miR-147-3p, miR-98-5p, and miR-10a-5p were mainly enriched in Wnt and MAPK inflammatory signaling. miR-10a-5p promoted the proliferation of mouse lung epithelial cells and downregulated the expression of Nfat5 and Map2k6. These data suggest SC-induced exosomal miRNAs might mediate the inflammatory signaling and might be involved in the SC treatment in asthma. The exosomal miRNAs might be promising candidates for the treatment of asthma.

Fibrillar assemblies by peptides are becoming one of the most promising nanomaterials due to their exceptional properties. The self-assembly of peptides into β sheets is a critical step in the fibrillization pathway. We investigated the length-dependent β-sheet growth mechanisms of polyalanine [poly(A)] peptides consisting of 6 to 24 alanines (A6 to A24) in water and on the hydrophobic surface, respectively, by molecular dynamics simulations. β-sheet growth behavior in water fits negative exponential growth model, showing that β-sheet growth rate decays exponentially with time. Meanwhile, increasing chain length leads to an accelerated decay of the β-sheet growth rate. By contrast, β-sheet growth on the surface from A6 to A18 occurs in two consecutive stages, both of which fit linear growth models. β-sheet growth rate in the first stage increases as chain length is increased, while the intermediate length peptide A12 has the highest β-sheet growth rate in the second stage. β-sheet growth behavior of A24 on the surface still fits negative exponential model. Overall, the hydrophobic surface accelerates β-sheet growth by enhancing local concentration and reducing conformational entropy of poly(A) peptide, and the β-sheet growth of the intermediate length peptide A12 is the fastest on the surface. Our simulation results shed light on understanding the accelerated peptide fibrillization on the hydrophobic surface.

"Yang-warming and kidney essence-replenishing" herbal paste could reduce cold-related asthma exacerbation.